A variety of mood disorders exist which compromise to varying degrees the social integration and quality of life of affected individuals. The major forms of mood disorder include bipolar disorder (manic depression) and unipolar disorders (major depression and unipolar mama). Other wood disorders include dysthymic disorder, cyclothymic disorder, seasonal affective disorder and substance-induced mood disorder.
Bipolar disorder is a common condition with a lifetime prevalence of 1.2% to 1.6% (Weissman et al. 1988, Psych. Med. 18:141–153; Kessler et al. 1994, Arch Gen. Psych. 51:8–19). It is characterised by recurrent episodes of mania and depression with symptomatic recovery between episodes.
The pathophysiology of bipolar disorder remains poorly understood despite considerable research (Goodwin et al. 1998, Arch. Gen. Psych. 55:23–25). Although it is strongly heritable, the genetics are complex, with less than fill concordance in monozygotic twins (Mitchell et al. 1993, Aust. & New Zeal. J. Psych. 27:560–580). At least four different susceptibility loci have been identified (Adams et al. 1998, Am. J. Hum. Genet; 62:10841091). A trait-dependent biological marker would assist genetic linkage studies (which are dependent upon the identification of the clinical phenotype) and would potentially lead to an understanding of the underlying molecular defect in bipolar disorder.
In unipolar depression, there are recurrent episodes of depression with symptomatic recovery, but there are no episodes of mania. In unipolar mania there are recurrent episodes of mania but no episodes of depression. Like bipolar disorder, the pathophysiology and specific genetic defects underlying unipolar disorders remain poorly understood.
Current techniques for diagnosing mood disorders rely entirely on subjective interpretation of a patient's condition based on clinical interview. However, apart from being relatively time-consuming, the subjective nature of this technique in interpreting a psychiatric profile does not provide consistently accurate determinations of clinical phenotype. Consequently, misdiagnosis of mood disorders may occur which can thereby affect the prescribed pharmacological and non-pharmacological therapy.
In the 1930s, Hunt and Guilford (1933, J. Abnormal and Social Psychology 28:443–452) found that hospitalised manic-depressive patients displayed slow alternation rates when viewing an ambiguous figure (ie. Wheatstone cube) compared to normal controls. The mean passive viewing number of alterations per minute was 4.25 for manic-depressives and 18.06 for normal controls. A strong implication from this study is that such slower alternation rates may be the result of clinical progression. Moreover, the data from this study support the use of this test to confirm the presence of manic-depressive illness in hospitalised individuals with a life history of illness at least as long as that for the individuals in the study.